An arrhythmia is an abnormal heart beat pattern. One example of arrhythmia is bradycardia wherein the heart beats at an abnormally slow rate or wherein significant pauses occur between consecutive beats. Other examples of arrhythmias include tachyarrhythmias wherein the heart beats at an abnormally fast rate. With atrial tachycardia, the atria of the heart beat abnormally fast. With ventricular tachycardia, the ventricles of the heart beat abnormally fast. Though often unpleasant for the patient, a tachycardia is typically not fatal. However, some types of tachycardia, particularly ventricular tachycardia, can trigger ventricular fibrillation wherein the heart beats chaotically such that there is little or no net flow of blood from the heart to the brain and other organs. Ventricular fibrillation, if not terminated within minutes, is fatal. Hence, it is highly desirable to prevent or terminate arrhythmias, particularly arrhythmias of the type that can lead to a ventricular fibrillation.
One technique for preventing tachycardias is to pace the heart at a rate somewhat faster than the intrinsic heart rate of the patient using a technique referred to as overdrive pacing. To help prevent a tachycardia from occurring, the stimulation device artificially paces the heart at an overdrive rate set to be slightly faster than the intrinsic heart rate of the patient. One particularly effective overdrive pacing technique, referred to herein as dynamic atrial overdrive (DAO) pacing, is described in U.S. Pat. No. 6,519,493 to Florio et al., entitled “Methods And Apparatus For Overdrive Pacing Heart Tissue Using An Implantable Cardiac Stimulation Device,” which is incorporated by reference herein. With DAO, the overdrive rate is controlled to remain generally uniform and, in the absence of a tachycardia, is adjusted upwardly or downwardly only occasionally. Dynamic overdrive techniques are also applicable to the ventricles and exemplary dynamic ventricular overdrive (DVO) techniques are described in U.S. patent applications: 1) Ser. No. 10/456,060 to Park et al., entitled “System And Method For Dynamic Ventricular Overdrive Pacing,” filed Jun. 6, 2003; and 2) Ser. No. 10/456,058, entitled “System And Method For Dynamic Ventricular Overdrive Pacing,” Jun. 6, 2003, which applications are also incorporated herein by reference.
It is believed that DAO and DVO are effective for at least some patients for preventing tachycardia for the following reasons. A normal, healthy heart typically beats only in response to electrical pulses generated from a portion of the heart referred to as the sinus node. The sinus node pulses are conducted to the various atria and ventricles of the heart via certain, normal conduction pathways. In some patients, however, additional portions of the heart also generate electrical pulses referred to as “ectopic” pulses. Each pulse, whether a sinus node pulse or an ectopic pulse has a refractory period subsequent thereto during which time the heart tissue is not responsive to any electrical pulses. A combination of sinus pulses and ectopic pulses can result in a dispersion of the refractory periods, which, in turn, can trigger a tachycardia. By overdrive pacing the heart at a generally uniform rate slightly above the intrinsic rate, the likelihood of the occurrence of ectopic pulses is reduced and the refractory periods within the heart tissue are rendered more uniform and periodic. Thus, the dispersion of refractory periods is reduced and the risk of tachycardia is reduced. Thus, overdrive pacing, particularly DAO and DVO, provides a useful technique for helping to prevent the onset of a tachycardia and for terminating a tachycardia should one nevertheless arise. Utilizing an overdrive algorithm in conjunction with multisite stimulation will also result in a collision of the electrical wavefronts further reducing dispersion of the refractory period effectively reducing the risk of tachycardia.
Herein, the term “overdrive pacing” generally refers to the sustained pacing of chambers of the heart at a rate higher than the intrinsic rate. Overdrive pacing can take the form of “preventive overdrive pacing”, which is employed for the purposes of preventing a tachycardia from occurring, and “therapeutic overdrive pacing”, which is employed for the purposes of terminating a tachycardia should one nevertheless arise. The overdrive rates associated with preventive overdrive pacing are much lower than those associated with therapeutic overdriving pacing.
Therapeutic overdrive pacing represents one type of antitachycardia pacing (ATP). Other ATP techniques have been developed as well that do not exploit overdrive pacing or at least do not exploit sustained overdrive pacing. The underlying principle of many such techniques is that if an implantable stimulation device delivers a stimulation pulse to the heart during a critical time period following a naturally occurring heartbeat during tachycardia, the tachycardia pathway will be rendered refractory abruptly terminating the tachycardia allowing the heart to revert to sinus, or natural, rhythm. In this regard, certain types of tachycardias are the result of an electrical feedback mechanism within the heart. For example, a natural heartbeat can occur through a normal pathway and re-enter through an alternate loop of tissue that perpetuates conduction (also known as an accessory or re-entrant pathway), thereby initiating a tachycardia. The delivery of a stimulation pulse causes the cardiac tissue in front of the stimulation pulse to depolarize (thereby causing the heart to contract), but leaves the tissue at the stimulation site refractory (i.e., the tissue cannot respond to additional stimulation). Thus, by injecting a stimulation pulse within the cardiac cycle, the stability of the feedback loop is disrupted and the tachycardia terminated thus allowing the heart may revert to a natural sinus rhythm.
One example is burst pacing (or “shotgunning”) wherein several sequential, rapid stimuli are delivered to the heart in an effort to terminate the tachycardia. The theory behind providing a burst of pulses is that sooner or later one of the stimulating pulses will occur at a time in the tachycardia cycle which will terminate the tachycardia (i.e. the pulse will occur during a “region of susceptibility”). Burst pacing may be delivered asynchronously or synchronously at a fixed, decreasing, or increasing, cycle length from a tachycardia complex until the tachycardia is terminated. Once the tachycardia has been terminated, the timing associated with the burst that succeeded in terminating the tachycardia may be stored and used as the starting point for applying a new burst of simulation pulses to the heart upon the next occurrence of a tachycardia. An alternate technique to find the termination window is by “scanning”, which is a type of burst pacing with variations in coupling interval. This technique utilizes an implantable stimulation device that automatically searches or “scans” for the pacing interval most likely to terminate a tachycardia. The implantable stimulation device delivers single or multiple stimulation pulses at “critically timed” coupling intervals and continues in a controlled sequence until the tachycardia terminates. For example, the controlled sequence may begin with a single stimulation pulse at one end of the scanning window and, with each successive tachycardia cycle, deliver additional pulses at increasing (or decreasing) coupling intervals in a controlled manner towards the other end of the window. Hence, the stimulation pulse scans through the scanning window looking for the region of susceptibility.
Exemplary patents describing ATP techniques include U.S. Pat. No. 6,101,414, to Mark Kroll, entitled “Method And Apparatus For Antitachycardia Pacing With An Optimal Coupling Interval,” and U.S. Pat. No. 5,431,689 to Weinberg et al., entitled “Implantable Stimulation System And Method For Terminating Cardiac Arrhythmias,” which are both incorporated by reference herein.
Regardless of the specific ATP technique, it has been found that ATP is most effective if applied early during the tachycardia. Unfortunately, conventional techniques for detecting the onset of a tachycardia do not detect the tachycardia as promptly as would be desired. One technique for detecting an atrial tachycardia is to monitor the atrial rate and initiate atrial ATP if the heart rate exceeds a certain threshold, typically referred to as an atrial tachycardia detection rate (ATDR). It may take a fair number of cardiac cycles, however, before the stimulation device can reliably detect a high atrial rate and, in particular, distinguish a high heart rate from a temporary shortening of an atrial heart rate interval caused by a premature beat such as a premature atrial contraction (PAC). It is also known to try to differentiate pathologic rhythms from normal physiologic rhythms by analyzing heart rate stability. Again, though, a fair number of cycles may be required before the stimulation device can reliably distinguish a change in heart rate stability caused by a tachycardia from one caused by premature beats or other transient factors. Conventional techniques for detecting a tachycardia are discussed in U.S. Pat. No. 5,109,842, to Adinolfi, entitled “Implantable Tachyarrhythmia Control System Having a Patch Electrode with an Integrated Cardiac Activity System.”
Also, care must be taken to ensure that ATP is not erroneously activated in circumstances where it is not needed and, in particular, in circumstances where it might be proarrhythmic. In this regard, in some patients, there are a large number of short nonsustained salvos of supraventricular tachycardia (SVT) or multiple sequential PACs which, if they occur during a post-ventricular atrial refractory period (PVARP), will not inhibit the atrial output thereby causing the atrial output to be delivered to a period of physiologic refractoriness in the atrial myocardium. Indeed, delivering a burst of ATP into a rhythm that would not have been sustained may be arrhythmogenic inducing atrial flutter or atrial fibrillation (AF) where this would not have occurred spontaneously. The need to avoid erroneous triggering of ATP often means that the tachycardia detection technique must process even more data before reliably concluding that a tachycardia has occurred.
Similar problems can arise in the detection of certain ventricular tachycardias. Failure to promptly detect a ventricular tachycardia (such as a low amplitude ventricular fibrillation (VF)) can result in a delay in the delivery of defibrillation shocks with a reduced likelihood of success. In this regard, it has been proposed to use the detection of loss of capture (LOC) of a series of ventricular pacing pulses as a means for detecting low amplitude VF and for triggering delivery of a high output defibrillation shock. See U.S. Pat. No. 5,350,401 to Levine, which is incorporated herein by reference. With that technique, upon detection of loss of capture of a ventricular pulse, the ventricular pulse output magnitude is increased and another pulse is delivered. If that pulse also fails to capture, the output magnitude is increased again. This process proceeds until either a ventricular pulse captures or until a maximum pulse output level is reached. If the maximum output is reached and the ventricular pulses still do not evoke capture, a determination is thereby made that a low amplitude VF may have occurred and a defibrillation shock may be delivered to terminate the VF. Although the technique is effective in eventually detecting low amplitude VF, the need to deliver a series of ventricular pulses with different pulse magnitudes delays the detection of VF, thus potentially reducing the effectiveness of subsequent shock therapy.
Thus, conventional atrial and ventricular tachycardia detection techniques do not always detect tachycardia as quickly as desired, resulting in a reduced likelihood that subsequent therapy will be successful. Accordingly, it would be desirable to provide improved techniques for promptly and reliably detecting atrial and ventricular tachycardias and aspects of the invention are generally directed to these ends. In particular, it would be desirable to provide techniques for exploiting the detection of loss of capture of backup pacing pulses in the detection of tachycardia. As will be explained below, loss of capture of backup pulses can be used to promptly detect a tachycardia.
The aforementioned problems associated with promptly detecting a tachycardia are even more problematic if preventive overdrive pacing were also to be performed. For example, in the technique where ATP is triggered based on intrinsic atrial rate, routine preventive overdrive pacing would prevent the device from continuously and reliably monitoring the intrinsic atrial rate. Using DAO, for example, the intrinsic atrial rate is not evaluated at all. Rather, increases or decreases in the overdrive rate are made based solely on the presence or absence of breakthrough beats. Alternatively, ATP could be triggered once the preventive overdrive pacing rate itself exceeds the ATDR, but it may take too many cycles before the overdrive rate is boosted up to that threshold. Also, as typically implemented, preventive atrial overdrive pacing rates never exceed the ATDR because the pacing device is programmed to never exceed a maximum overdrive rate that is set well below the ATDR. Likewise, techniques based on heart rate stability are not easily and effectively implemented during preventive overdrive pacing.
For these and other reasons, most conventional pacing devices do not provide for both preventive overdrive pacing and ATP. In devices that do provide for both (see, for example, the AT500 pacemaker provided by Medtronic Corporation of Minneapolis, Minn., USA), it does not appear that ATP is triggered as promptly as desired and so may not provide optimal termination of the tachycardia. Accordingly, it also would be desirable to provide improved techniques promptly switching from preventive overdrive pacing to ATP and additional aspects of the invention are directed to these ends.
In view of the risks associated with delivering ATP during arrhythmias that otherwise would not be sustained (such as where burst ATP might actually induce atrial flutter or fibrillation), it also would be desirable to provide techniques for determining whether to enable automatic switching of preventive overdrive pacing to ATP within a particular patient and still other aspects of the invention are directed to that end.